Host-parasite local adaptation after experimental coevolution of Caenorhabditis elegans and its microparasite Bacillus thuringiensis

Coevolving hosts and parasites can adapt to their local antagonist. In studies on natural populations, the observation of local adaptation patterns is thus often taken as indirect evidence for coevolution. Based on this approach, coevolution was previously inferred from an overall pattern of either parasite or host local adaptation. Many studies, however, failed to detect such a pattern. One explanation is that the studied system was not subject to coevolution. Alternatively, coevolution occurred, but remained undetected because it took different routes in different populations. In some populations, it is the host that is locally adapted, whereas in others it is the parasite, leading to the absence of an overall local adaptation pattern. Here, we test for overall as well as population-specific patterns of local adaptation using experimentally coevolved populations of the nematode Caenorhabditis elegans and its bacterial microparasite Bacillus thuringiensis. Furthermore, we assessed the importance of random interaction effects using control populations that evolved in the absence of the respective antagonist. Our results demonstrate that experimental coevolution produces distinct local adaptation patterns in different replicate populations, including host, parasite or absence of local adaptation. Our study thus provides experimental evidence of the predictions of the geographical mosaic theory of coevolution, i.e. that the interaction between parasite and host varies across populations.     

Mixed-mode loading of the cement-bone interface: a finite element study

While including the cement-bone interface of complete cemented hip reconstructions is crucial to correctly capture their response, its modelling is often overly simplified. In this study, the mechanical mixed-mode response of the cement-bone interface is investigated, taking into account the effects of the well-defined microstructure that characterises the interface. Computed tomography-based plain strain finite element analyses models of the cement-bone interface are built and loaded in multiple directions. Periodic boundaries are considered and the failure of the cement and bone fractions by cracking of the bulk components are included. The results compare favourably with experimental observations. Surprisingly, the analyses reveal that under shear loading no failure occurs and considerable normal compression is generated to prevent interface dilation. Reaction forces, crack patterns and stress fields provide more insight into the mixed-mode failure process. Moreover, the cement-bone interface analyses provide details which can serve as a basis for the development of a cohesive law.     

Implementation of asymmetric yielding in case-specific finite element models improves the prediction of femoral fractures

Although asymmetric yielding in bone is widely shown in experimental studies, previous case-specific non-linear finite element (FE) studies have mainly adopted material behaviour using the Von Mises yield criterion (VMYC), assuming equal bone strength in tension and compression. In this study, it was verified that asymmetric yielding in FE models can be captured using the Drucker-Prager yield criterion (DPYC), and can provide better results than simulations using the VMYC. A sensitivity analysis on parameters defining the DPYC (i.e. the degree of yield asymmetry and the yield stress settings) was performed, focusing on the effect on bone failure. In this study, the implementation of a larger degree of yield asymmetry improved the prediction of the fracture location; variations in the yield stress mainly affected the predicted failure force. We conclude that the implementation of asymmetric yielding in case-specific FE models improves the prediction of femoral bone strength.     

Solid-solid interface adsorption of proteins and enzymes in nanophase-separated amphiphilic conetworks

Amphiphilic polymer conetworks (APCNs) are materials with a very large interface between their hydrophilic and hydrophobic phases due to their nanophase-separated morphologies. Proteins were found to enrich in APCNs by up to 2 orders of magnitude when incubated in aqueous protein solutions, raising the question of the driving force of protein uptake into APCNs. The loading of poly(2-hydroxyethyl acrylate)-linked by-poly(dimethylsiloxane) (PHEA-l-PDMS) with heme proteins (myoglobin, horseradish peroxidase, hemoglobin) and lipases was studied under variation of parameters such as incubation time, pH, concentration of the protein solution, and conetwork composition. Adsorption of enzymes to the uncharged interface is the main reason for protein uptake, resulting in protein loading of up to 23 wt %. Experimental results were supported by computation of electrostatic potential maps of a lipase, indicating that hydrophobic patches are responsible for the adsorption to the interface. The findings underscore the potential of enzyme-loaded APCNs in biocatalysis and as sensors.     

Loss of heterozygosity at an unlinked genomic locus is responsible for the phenotype of a Candida albicans sap4Δ sap5Δ sap6Δ mutant

The diploid genome of the pathogenic yeast Candida albicans exhibits a high degree of heterozygosity. Genomic alterations that result in a loss of heterozygosity at specific loci may affect phenotypes and confer a selective advantage under certain conditions. Such genomic rearrangements can also occur during the construction of C. albicans mutants and remain undetected. The SAP2 gene on chromosome R encodes a secreted aspartic protease that is induced and required for growth of C. albicans when proteins are the only available nitrogen source. In strain SC5314, the two SAP2 alleles are functionally divergent because of differences in their regulation. Basal expression of the SAP2-2 allele, but not the SAP2-1 allele, provides the proteolytic degradation products that serve as inducers for full SAP2 induction. A triple mutant lacking the SAP4, SAP5, and SAP6 genes, which are located on chromosome 6, has previously been reported to have a growth defect on proteins, suggesting that one of the encoded proteases is required for SAP2 expression. Here we show that this sap4Δ sap5Δ sap6Δ mutant has become homozygous for chromosome R and lost the SAP2-2 allele. Replacement of one of the SAP2-1 copies in this strain by SAP2-2 and its regulatory region restored the ability of the sap4Δ sap5Δ sap6Δ mutant to utilize proteins as the sole nitrogen source. This is an illustrative example of how loss of heterozygosity at a different genomic locus can cause the mutant phenotype attributed to targeted deletion of a specific gene in C. albicans.